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首页> 外文期刊>Infection and immunity >Role of Sulfated Glycans in Adherence of the Microsporidian Encephalitozoon intestinalis to Host Cells In Vitro
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Role of Sulfated Glycans in Adherence of the Microsporidian Encephalitozoon intestinalis to Host Cells In Vitro

机译：硫酸聚糖在体外微孢子虫脑小肠粘附宿主细胞中的作用。

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Microsporidia are obligate intracellular opportunistic protists that infect a wide variety of animals, including humans, via environmentally resistant spores. Infection requires that spores be in close proximity to host cells so that the hollow polar tube can pierce the cell membrane and inject the spore contents into the cell cytoplasm. Like other eukaryotic microbes, microsporidia may use specific mechanisms for adherence in order to achieve target cell proximity and increase the likelihood of successful infection. Our data show that Encephalitozoon intestinalis exploits sulfated glycans such as the cell surface glycosaminoglycans (GAGs) in selection of and attachment to host cells. When exogenous sulfated glycans are used as inhibitors in spore adherence assays, E. intestinalis spore adherence is reduced by as much as 88%. However, there is no inhibition when nonsulfated glycans are used, suggesting that E. intestinalis spores utilize sulfated host cell glycans in adherence. These studies were confirmed by exposure of host cells to xylopyranoside, which limits host cell surface GAGs, and sodium chlorate, which decreases surface sulfation. Spore adherence studies with CHO mutant cell lines that are deficient in either surface GAGs or surface heparan sulfate also confirmed the necessity of sulfated glycans. Furthermore, when spore adherence is inhibited, host cell infection is reduced, indicating a direct association between spore adherence and infectivity. These data show that E. intestinalis specifically adheres to target cells by way of sulfated host cell surface GAGs and that this mechanism serves to enhance infectivity.
机译：微孢子虫是专一性的细胞内机会生物，其通过耐环境的孢子感染包括人类在内的多种动物。感染需要使孢子紧贴宿主细胞，以便空心极管可以刺穿细胞膜并将孢子内容物注入细胞质中。像其他真核微生物一样，微孢子虫可能会使用特定的粘附机制，以实现靶细胞接近并增加成功感染的可能性。我们的数据表明， Encephalitozoon intestinalis 在宿主细胞的选择和附着中利用了硫酸化聚糖，例如细胞表面的糖胺聚糖（GAG）。当在孢子粘附试验中使用外源硫酸化聚糖作为抑制剂时， E。肠内孢子附着力降低多达88％。然而，当使用非硫酸化聚糖时，没有抑制作用，表明是 E。小肠孢子利用硫酸化的宿主细胞聚糖进行粘附。这些研究已通过将宿主细胞暴露于吡喃吡喃糖苷（可限制宿主细胞表面GAG）和氯酸钠（降低表面硫酸化）而得到证实。对表面GAGs或表面硫酸乙酰肝素缺乏的CHO突变细胞系的孢子粘附研究也证实了硫酸化聚糖的必要性。此外，当孢子粘附被抑制时，宿主细胞感染减少，表明孢子粘附和感染性之间直接相关。这些数据显示 E。小肠通过硫酸化的宿主细胞表面GAGs特异性粘附于靶细胞，这种机制有助于增强感染性。

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